Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Having -c- – wherein x is chalcogen – bonded directly to...
Reexamination Certificate
2000-05-31
2001-08-14
Henley, III, Raymond (Department: 1614)
Drug, bio-affecting and body treating compositions
Designated organic active ingredient containing
Having -c-, wherein x is chalcogen, bonded directly to...
C514S561000, C514S562000, C514S565000
Reexamination Certificate
active
06274612
ABSTRACT:
FIELD OF THE INVENTION
The present invention pertains to the treatment of immunological disorders, including more particularly to the treatment of autoimmune disorders.
BACKGROUND
Autoimmune disease is caused when one's own immune system incorrectly attacks one's own tissue. It is known to treat patients suffering from autoimmune disorders by intravenously introducing immunoglobulin into the patients. A period of remission in the disease can be produced by this treatment. Although the use of immunoglobulin has been relatively effective in the treatment of autoimmune disorders, the mechanism of action is unknown. The intravenous administration of immunoglobulin (IVIG) to any particular patient may cause side effects, such as fever and muscle aches, headaches, nausea and vomiting, dizziness, and tachycardia. There is also the potential of transferring to the patient disease from the person who donated blood used for the manufacture of this immunoglobulin. At a cost of approximately $100/gram, treatment with immunoglobulin is also relatively expensive, amounting to many thousands of dollars for each treatment. There has recently been a shortage in the availability of IVIG.
Standardized parenteral nutritional protocols, which include a combination of amino acids, have been traditionally given to nourish patients who could not be fed orally or gastrically. In one such case, I had used a standardized parenteral nutritional protocol to nourish a patient who had been suffering from an autoimmune disease. The patient, a 70-year old female weighing approximately 40 kg, presented herself to me in 1990 with generalized weakness and ptosis (drooping of the eyelids). The diagnosis of Myasthenia Gravis without Thymoma, an autoimmune disorder, was made following a Tensilon test of the thenar muscle and elevated Acetylcholine receptor antibody titer measured in the blood. The Acetylcholine receptor antibody causes muscle weakness by attacking the muscle endplate, thus interfering with the Acetylcholine synapse between the nerve and the muscle.
The patient regained good strength on a combination of Pyridostigmine and Prednisone, drugs which have been traditionally used to treat the symptoms of Myasthenia Gravis by respectively making more acetylcholine available at the muscle endplate and by reducing the inflammatory response at the muscle end plate plus reducing the amount of antibody formation. The daily administration of Pyridostigmine and Prednisone were continued in order to maintain reasonable control of the symptoms of the disease.
On Nov. 6, 1992, the patient underwent a bowel operation for the correction of an enterorectal fistula. On Nov. 8, 1992, because of her inability to be orally or gastrically fed, the patient was intravenously administered a standardized parenteral nutritional protocol, which was continued for six days until she was discharged from the hospital on Nov. 14, 1992. No change in the patient's Myasthenia Gravis status was noted at this time. As the patient was able to be orally fed, she was not administered the standardized parenteral nutritional protocol after discharge from the hospital. To maintain control of the effects of the Myasthenia Gravis, the patient was continued on Pyridostigmine and Prednisone.
On Nov. 26, 1992, the patient suffered from abdominal discomfort and tenderness and was readmitted to the hospital. Oral feeding ceased, and on Nov. 27, 1992 (Day 1 of the intravenous feeding), I again administered the standardized parenteral nutritional protocol (First Protocol) to the patient at a rate of 100 cc. per hour. The composition of this protocol with the appropriate quantities of each element is set forth in Table 1.
TABLE 1
Individual Elements and the Quantity of each Element in
100 cc of a First Standardized Parenteral Nutritional Protocol
Elements
Amount
Distilled Water
Essential Amino Acids
Isoleucine USP
0.21
gms
Leucine USP
0.27
gms
Lysine as Lysine acetate USP
0.31
gms
Methionine USP
0.16
gms
Phenylalanine USP
0.17
gms
Threonine USP
0.046
gms
Valine USP
0.2
gms
Non-Essential Amino Acids
Alanine USP
0.21
gms
Arginine USP
0.29
gms
Histidine UAP
0.085
gms
Proline USP
0.34
gms
Serine USP
0.18
gms
Glycine USP
0.42
gms
Cystein USP
0.014
gms
Lipids
10
gms
Soybean Oil
*
Egg Phosphatides
*
Electrolytes
Sodium Chloride
80
mEq/liter
Sodium Phossphate
25
mEq/liter
Potassium Chloride
30
mEq/liter
Calcium Gluconate
12
mEq/liter
Magnesium Sulfate
8
mEq/liter
Zinc Sulfate
20
mEq/liter
Trace Elements
Zinc
5
mg
Copper
2
mg
Manganese
0.5
mg
Chromium
10
mcg
Selenium
60
mcg
Daily Vitamins
Ascorbic Acid
500
mg
Vitamin A
1000
i.u.
Vitamin D
1000
i.u.
Thiamine
50
mg
Riboflavin
10
mg
Pyridoxine
5
mg
Niacin
100
mg
Vitamin E
5
i.u.
Dexpanthenol
25
mg
Vitamin K
10
mg
On Day 3 of the intravenous feeding, the patient felt much stronger and continued to feel strong for several days thereafter despite having an elevated Acetylcholine receptor antibody titer of 25, with less than 0.5 being normal.
On Day 5 of the intravenous feeding, the patient developed a cholinergic attack secondary to the Pyridostigmine that was continuously administered to her. This resulted in abdominal cramping. The cholinergic attack was relieved by the intravenous administration of Atropine, which countered the effect of Pyridostigmine. The administration of the Pyridostigmine and Prednisone to the patient was discontinued.
On Day 6 of the intravenous feeding, the patient felt strong, despite the discontinuation of the Pyridostigmine and Prednisone.
On Day 7 of the intravenous feeding, the patient continued to get stronger despite the fact that her Acetylcholine receptor antibody titer had risen to 30, a level that typically results in weakness. This indicated to me that the Myasthenia Gravis was not being controlled by the reduction of the Acetylcholine receptor antibody titer, a result typically achieved by the administration of Prednisone, but rather by blocking the effects of the Acetylcholine receptor antibody. Since the administration of the Pyridostigmine had been discontinued, this indicated to me that the effect of the high Acetylcholine receptor antibody titer on the muscle endplates was being countered by the intravenous administration of the First Protocol.
The patient was discharged from the hospital on Dec. 14, 1992, after which she was continued on the First Protocol until Mar. 23, 1993. During this period, the patient's Acetylcholine receptor antibody titer had been measured at 57, 38, and 30 on the respective dates of Jan. 4, 1993, Jan. 25, 1993 and Feb. 18, 1993.
The patient's Myasthenia Gravis continued in remission until Mar. 31, 1993, eight days after the intravenous feeding was discontinued. Two days later, on Apr. 2, 1993, the patient was continued on Pyridostigmine 30 mg twice a day and the patient regained her strength. Although the effects of Myasthenia Gravis typically had to be controlled by a combination of Pyridostigmine and Prednisone, the patient's Myasthenia Gravis continued in partial remission for over 5 months necessitating the use of only Pyridostigmine without the administration of Prednisone. This indicated to me that the intravenous administration of the First Protocol had a prolonged positive effect in treating the Myasthenia Gravis.
On Sep. 13, 1993, the patient had increased weakness and was administered Prednisone 40 mg daily, in addition to the Pyridostigmine. A week later the Prednisone was reduced to 20 mg every other day. The patient was continued on this combination of Pyridostigmine and Prednisone, a treatment that was similar to that given to her prior to the bowel operation. The patient's Acetylcholine receptor antibody titer was measured at 28.7 on Aug. 11, 1993, and at 14 on Oct. 23, 1993, at which time the patient had been continuously administered Prednisone. The patient remained strong until Feb. 1997.
SUMMARY OF THE INVENTION
Through my review of the observations in this case in 1992-1993 I discovered that the administration of the First Protocol to this patient may not only have nourished the patient, but a
Henley III Raymond
Lyon & Lyon LLP
LandOfFree
Method of treating an autoimmune disorder does not yet have a rating. At this time, there are no reviews or comments for this patent.
If you have personal experience with Method of treating an autoimmune disorder, we encourage you to share that experience with our LandOfFree.com community. Your opinion is very important and Method of treating an autoimmune disorder will most certainly appreciate the feedback.
Profile ID: LFUS-PAI-O-2478521